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Biomedical subjects

O Uyama

Publications and source records attributed to O Uyama.

At least 19 recordsLinked to original sources
PubMed2001

Orthostatic hypotension in elderly persons during passive standing: a comparison with young persons.

BACKGROUND: The present study was aimed at clarifying the mechanism of orthostatic hypotension (OH) that occurs in elderly persons and at investigating assisting methods to prevent OH by evaluating changes in autonomic nervous system (ANS) activity and cerebral circulation of elderly persons when engaged in passive standing. METHODS: Eight elderly volunteers and 9 young volunteers gave informed consent to participate in the study. Two experimental conditions were established: (i) "active standing," in which the subjects stood on their own with guidance from an assistant, and (ii) "passive standing," in which the subjects were placed in a standing position completely by an assistant. ANS was determined before and after standing by measuring the heart rate variability. The reaction of the ANS was evaluated on the basis of low-frequency power (LF: 0.05--0.15 Hz) and high-frequency power (HF: 0.15--0.4 Hz), which were separated from the R-R interval data by power spectral analysis using the fast Fourier transformation. Cerebral perfusion was measured over the right frontal region using a near-infrared spectroscopy cerebral oxygen monitor. RESULTS: The main findings were: (i) Transient decreases in blood pressure occurred immediately after standing in both the young and elderly subjects. (ii) The LF:HF ratio increased significantly ( p <.05) immediately after active standing in the young subjects, whereas this ratio increased in the elderly subjects after some delay. (iii) The LF:HF ratio increased significantly ( p <.01) immediately after passive standing in the young subjects, whereas this ratio decreased significantly ( p <.05) in the elderly subjects. (iv) In the elderly subjects, the total hemoglobin (HbT) and oxyhemoglobin showed the greatest decrease during the 15-second period after standing. The maximum changes in the HbT with passive standing differed significantly ( p <.01) from those observed during active standing. CONCLUSIONS: Our findings emphasize the need to devise bioengineered means that allow elderly persons to exert themselves, to maintain or improve muscle contractility and ANS function, while providing minimum assistance for standing.

Adult↗
PubMed1997

Bone changes and carotid atherosclerosis in postmenopausal women.

BACKGROUND AND PURPOSE: Because of increased life expectancy, most postmenopausal women today suffer from osteoporosis and atherosclerotic diseases, which are currently considered unrelated diseases. Our study was aimed at analyzing relations between bone mineral density (BMD) and ultrasonographic assessment of carotid wall characteristics. METHODS: The relation of carotid atherosclerosis to BMD was examined in 30 postmenopausal women aged 67 to 85 years. High-resolution B-mode ultrasonography was performed, and the severity of carotid atherosclerosis was determined by plaque score. BMD was measured by dual-energy x-ray absorptiometry. RESULTS: The correlation of plaque score with low total BMD was r = .549 (P < .002). Multiple linear regression analysis indicated significant correlation of plaque score with total cholesterol level and low total BMD. CONCLUSIONS: Our results suggest a relation between carotid atherosclerosis, one of the major causes of ischemic cerebrovascular diseases, and osteoporosis.

Absorptiometry, Photon↗
PubMed1995

Prostate cancer-induced oncogenic hypophosphatemic osteomalacia.

A 65-year-old male with prostate carcinoma showed mild hypocalcemia of 7.9 mg/dl, marked hypophosphatemia of 1.7 mg/dl, hyperphosphaturia (tubular reabsorption of phosphorus 43% and tubular threshold for phosphorus of 0.6 mg/dl), low serum 1,25 (OH)2D level of less than 5 pg/ml and osteomalacia indicated by a marked increase of relative osteoid volume and fractional formation rate in the undecalcified section. Oncogenic osteomalacia due to prostatic carcinoma with suppression of 1,25 (OH)2D production and phosphaturia was suggested.

Adenocarcinoma↗
PubMed1995

Role of eosinophils and cell adhesion molecules in the allergen-induced asthmatic response of rats.

To evaluate the airway infiltration of eosinophils in the asthmatic responses of Brown-Norway rats, which were sensitized with ovalbumin, the time course of eosinophil infiltration and respiratory resistance (Rrs) after ovalbumin challenge was measured. The effect of treatment with monoclonal antibody against ICAM-1 and CD18 was studied. Finally, the expression of ICAM-1 and CD18 in the airway was investigated. All rats showed Rrs increase 6-7 hours after ovalbumin challenge, indicating a late asthmatic response (LAR). Animals with LAR had higher eosinophil counts than those with an immediate asthmatic response (IAR) and in the sensitized but nonchallenged animals. Rats treated with the antibodies showed significantly smaller increases in Rrs and lower eosinophil counts than the control animals. Immunohistochemical staining in airway was performed. ICAM-1 immunoreactivity was positive on both the epithelium and the vascular endothelium of a trachea section, and on the pulmonary vascular endothelium. ICAM-1 expression was upregulated after challenge. The number of CD18-positive cells in sections of trachea and lung increased after challenge. Our results show that eosinophil infiltration is important in LAR development and the treatment with antagonists of ICAM-1 and CD18 may provide a therapeutic approach to reducing asthmatic symptoms.

Aerosols↗
PubMed1994

Risk factors for carotid atherosclerosis and platelet activation.

Thromboxane A2 biosynthesis was studied in healthy subjects, in patients in whom the extent of carotid atherosclerosis was determined, and in patients receiving chronic aspirin treatment, to determine what factors activate platelets to develop carotid atherosclerosis. Urinary 11-dehydrothromboxane B2, a major metabolite of thromboxane A2, was measured by radioimmunoassay after purification by reverse-phase HPLC. The extent of carotid atherosclerosis was determined by real-time B-mode ultrasonography. The severity of carotid atherosclerosis in each subject was evaluated by plaque score, which was computed by summing the maximum thickness of plaque measured in millimeters. Urinary excretion of 11-dehydrothromboxane B2 in healthy subjects was higher (P < 0.01) in cigarette smokers (1063 +/- 244 ng/g creatinine) than in non-smokers (815 +/- 183 ng/g creatinine). Aspirin significantly suppressed 11-dehydrothromboxane B2 excretion (266 +/- 114 ng/g creatinine). In the 24 patients in whom the plaque score was measured, multivariate analysis indicated a significant positive correlation between urinary excretion of 11-dehydrothromboxane B2 and plaque score, age, smoking and hypercholesteremia. Our results indicate that risk factors such as age, hypercholesteremia, atherosclerosis and smoking activate platelets in vivo to develop carotid atherosclerosis.

Adult↗
PubMed1994

[Role of eosinophils and cell adhesion molecules in the asthmatic response to allergen].

To evaluate the eosinophil infiltration in lung tissues in asthmatic responses of Brown-Norway rats and guinea pigs, both of which were sensitized with ovalbumin (OA), the time course of changes in respiratory impedance (Zrs) and eosinophil influx after aerosol challenge with OA were measured. The effect of treatment with monoclonal antibody (MoAb) 1A29 against rat intercellular adhesion molecule-1 (ICAM-1) alone and a mixture of MoAb 1A29 and MoAb WT-3 against rat CD18 on asthmatic responses of the rats was studied. Finally, these expressions in lung tissues of the rats were recognized. The number of eosinophils in the subepithelial area was counted in sections of lung tissue stained with Giemsa's solution, using an Interaktive Build-Analyse System (IBAS). All of the rats and 80% of the guinea pigs developed an increase in Zrs 6-7 hours after challenge, indicating that these animals showed a late asthmatic response (LAR). The rats and the guinea pigs with a LAR had higher eosinophil counts than those with an immediate asthmatic response and sensitized, non-challenged animals (p < 0.01). The rats treated with MoAb 1A29 alone (n = 5) and a mixture of MoAb 1A29 and MoAb WT-3 (n = 8) developed significantly smaller increases in Zrs and a smaller eosinophil influx than the control animals treated with phosphate buffered saline (n = 15): 147.3 +/- 3.5, 134.8 +/- 11.6 versus 158.8 +/- 6.3% of baseline; 734 +/- 21, 545 +/- 108 versus 1006 +/- 147 cells/mm2 (p < 0.01). Immunoperoxidase staining of rat lung tissues using MoAb 1A29 or MoAb WT-3 was performed ICAM-1 immunoreactivity was positive in the basilar portion of the epithelium, in the vascular endothelium of the trachea and in the pulmonary vascular endothelium. ICAM-1 immunoreactivity was revealed to be upregulated after challenge. The number of CD18-positive cells in the trachea and in the subepithelial area increased after challenge. These results show that eosinophil infiltration corresponds closely to bronchoconstriction in LAR and that treatment with MoAbs to ICAM-1 and CD18 may be effective in reducing asthmatic symptoms.

Airway Resistance↗
PubMed1993

Determinants of relative amounts of medullary organic osmolytes: effects of NaCl and urea differ.

Sorbitol, inositol, betaine, taurine, and glycerophosphorylcholine (GPC) are organic osmolytes that accumulate in the renal inner medulla during antidiuresis. In the cultured cell model, high medium sodium increases all the cell osmolytes and high medium urea increases cell GPC and inositol. It has been difficult, however, to discriminate between the effects of sodium and urea on organic osmolytes in water-deprived animals. To determine the nature of the in vivo responses of osmolyte accumulation induced by extracellular sodium or urea, we measured the medullary organic osmolytes and tested the degree of their linear correlation with urine and tissue parameters in control, dehydrated, salt-loaded, and urea-loaded rats. All of the osmolytes except myo-inositol increased in salt-loaded rats. Betaine and sorbitol contents in dehydrated rats were less than in salt-loaded rats, but other osmolytes increased significantly. Conversely, in urea-loaded rats, only GPC increased significantly, whereas either no change occurred for other osmolytes or sometimes betaine and sorbitol levels decreased. These data suggest that high sodium increases all of the osmolytes except myoinositol, whereas high urea increases only GPC and may decrease the renal medullary contents of betaine and sorbitol. We also demonstrated, using linear regression analysis, that urea and electrolyte in urine as well as tissue correlate well with each osmolyte measured.

Animals↗
PubMed1993

Do anger and aggression affect carotid atherosclerosis?

BACKGROUND AND PURPOSE: Although a number of metabolic and psychosocial factors have been identified as coronary risk factors, no studies have evaluated the relation between personality and cerebrovascular disease. The purpose of the present study was to elucidate the relation between the characteristics of anger or aggression and the severity of carotid atherosclerosis on the basis of the findings of B-mode ultrasonography. METHODS: The Cornell Medical Index was used to measure anger in 34 patients with signs of atherosclerosis or at least one of four recognized risk factors for atherosclerosis (hypertension, hypercholesterolemia, diabetes mellitus, and cigarette smoking). The Rosenzweig Picture Frustration Study and Yatabe-Guilford Personality Test were used to evaluate aggression. High-resolution B-mode ultrasonography was performed, and the severity of carotid atherosclerosis was determined by plaque score. The occurrence of risk factors for carotid atherosclerosis was compared among the patients. RESULTS: The correlation of plaque score with one item that endorses anger was r = .65 (P < .01) and with "extrapersistive" in aggression was r = .50 (P < .01). Multivariate analysis identified significant correlations between plaque score and age, hypercholesterolemia, and anger. CONCLUSIONS: Our results suggest that anger and, perhaps, aggression may be risk factors for cerebrovascular disease.

Aggression↗
PubMed1993

Distinct responses of interleukin-6 and other laboratory parameters to treatment in a patient with Wegener's granulomatosis.

We describe a patient with Wegener's granulomatosis in whom the serum levels of interleukin-6 (IL-6) and other laboratory parameters were monitored. The IL-6 and CRP levels, which were extremely high before treatment, declined rapidly with corticosteroid and cyclophosphamide. IgG, leukocyte count and platelet count declined more gradually. Thus, determination of the serum IL-6 level might be useful in diagnosing and monitoring Wegener's granulomatosis.

Biomarkers↗
PubMed1993

Niceritrol reduces plasma lipoprotein(a) levels in patients undergoing maintenance hemodialysis.

Lp(a) is an LDL-like lipoprotein carrying the apoprotein(a) glycoprotein and has recently been recognized to be an independent risk factor for coronary heart disease. We studied plasma Lp(a) levels in 40 patients undergoing maintenance hemodialysis (24 male, 16 female; aged 16-83 years). Fasting plasma Lp(a) levels were measured by an enzyme-linked immunosorbent assay. The median value of plasma Lp(a) concentrations in hemodialysis patients was significantly higher than that of the normal volunteers (26.0 +/- 2.7 vs. 10.8 +/- 3.7 mg/dL, p < .05). Lp(a) levels did not correlate with age, duration of hemodialysis, total cholesterol, triglyceride, HDL cholesterol, or LDL cholesterol. The 11 patients whose plasma Lp(a) concentrations exceeded 20 mg/dL received niceritrol, a prodrug of nicotinic acid, at a dosage of 500 mg t.i.d. for 4 weeks. The plasma Lp(a) levels were significantly lower after 4 weeks of treatment (38.3 +/- 4.2 vs. 31.5 +/- 3.2 mg/dL, p < .01).

Adult↗
PubMed1993

[Superoxide dismutase suppressed asthmatic response with inhibition of manganese superoxide induction in rat lung].

To investigate the involvement of oxygen radicals in the development of asthma, we examined the time course of changes in the expression of superoxide dismutases (SODs) both at mRNA and protein levels in the rat model of allergic asthma. We then examined the effects of recombinant-human SOD (r-hSOD) on these expressions and on the late asthmatic response (LAR). 1) In situ hybridization histochemistry and immunocytochemistry revealed that non-sensitized and sensitized rats before challenge had a very low level of manganese SOD (MnDOS) in the bronchial epithelial cells, although they showed a significant level of copper-zinc SOD (CuZnSOD). 2) All of the animals displayed LAR within 7 hours after the challenge, when they showed dramatic induction of MnSOD, but not of CuZnSOD, in the epithelial cells. 3) Treatment with r-hSOD almost completely suppressed LAR, with abolishment of MnSOD induction. This study suggests that the oxygen radical plays an important role in the inflammatory state of bronchial asthma, during which some cytokines induce the expression of MnSOD in the lung.

Animals↗
PubMed1992

Protective effects of human recombinant superoxide dismutase on transient ischemic injury of CA1 neurons in gerbils.

BACKGROUND AND PURPOSE: It has been postulated that oxygen-derived free radicals are produced in significant quantities upon reperfusion of ischemic brain and that the free radicals play a pivotal role in triggering the ischemic neuronal damage causing delayed neuronal death. This study was undertaken to examine the effects of human recombinant superoxide dismutase on the delayed neuronal death of CA1 neurons and on the change in the expression of messenger ribonucleic acid for endogenous copper-zinc superoxide dismutase after transient ischemia. METHODS: Human recombinant superoxide dismutase (8 x 10(5) units/kg) or apo-superoxide dismutase was administered intravenously 1 minute before bilateral carotid artery occlusion in gerbils divided among four experimental groups. Endogenous copper-zinc superoxide dismutase messenger ribonucleic acid was analyzed by in situ hybridization histochemistry using a sulfur-35-labeled oligonucleotide probe. Immunohistochemical localizations of administered human recombinant superoxide dismutase were investigated. RESULTS: All gerbils receiving apo-superoxide dismutase exhibited almost complete destruction of CA1 neurons 7 days after 5 minutes of ischemia. The gerbils treated with human recombinant superoxide dismutase showed mild lesions (p less than 0.01). Discrete localizations were observed for endogenous copper-zinc superoxide dismutase messenger ribonucleic acid. Transient ischemia increased labeling throughout the hippocampus after 30 minutes and 24 hours of reperfusion. This increase was abolished by treatment with human recombinant superoxide dismutase. This phenomenon was confirmed by Northern blot analysis. The interneurons in CA3 and cells in the hilus were mainly stained against administered superoxide dismutase at 5 and 30 minutes, and these reactions had disappeared at 20 hours after the administration. CONCLUSIONS: Our data demonstrate protective effects of human recombinant superoxide dismutase against ischemic neuronal damage and support the hypothesis that the generated free radicals induce a vicious cycle leading to delayed neuronal death.

Animals↗
PubMed1992

Urinary 11-dehydro-thromboxane B2: a quantitative index of platelet activation in cerebral infarction.

Thromboxane A2 (TXA2) biosynthesis was studied in healthy subjects, patients with chronic cerebral infarction, patients under chronic aspirin treatment and patients with atrial fibrillation. Urinary 11-dehydro-TXB2, as a major metabolite of TXA2, was measured by radioimmunoassay. The extent of carotid atherosclerosis was determined by B-mode ultrasonography. The mean +/- SD urinary excretion in patients with cerebral infarction and distinct carotid-atherosclerotic lesions (1,725 +/- 239 ng/g creatinine, n = 6) was significantly higher (p less than 0.01) than in healthy subjects (911 +/- 239 ng/g creatinine, n = 44) and patients with cerebral infarction who had no distinct carotid lesion (1,050 +/- 191 ng/g creatinine, n = 6). The urinary excretion of healthy subjects was higher (p less than 0.01) in smokers (1,063 +/- 244 ng/g creatinine, n = 17) than in non-smokers (815 +/- 183 ng/g creatinine, n = 27). Aspirin largely suppressed 11-dehydro-TXB2 excretion (266 +/- 114 ng/g creatinine, n = 7). Three of 5 patients with atrial fibrillation showed very high values. Our results indicated that platelet activation occurs in the atherosclerotic lesions, and that urinary 11-dehydro-TXB2 is the appropriate analytic target for detecting platelet activation.

Adult↗
PubMed1992

Decreased sodium dependent D-glucose transport across renal brush-border membranes in cis-diamminedichloride platinum induced acute renal failure.

Na-coupled D-glucose transport in rabbits with cis-diamminedichloride platinum (CDDP; cisplatin) induced acute renal failure (ARF) has been studied. ARF occurred at 3 days after injection of CDDP (3 mg/kg i.v.). Na-coupled D-glucose transport into brush-border membrane vesicles (BBMV) from both outer cortex (OC) and outer medulla (OM) of ARF rabbits under zero-trans condition was decreased. Increased Km (i.e., decreased affinity of transport carrier for D-glucose) in OC and decreased Vmax (i.e., decreased number of glucose carrier) in OM were observed in CDDP-induced ARF rabbits. Decrease glucose transport was also observed under equilibrium exchange condition. Intravesicular volume of BBMV from OC and OM of ARF rabbits was decreased. In homogenate and BBMV from OC and OM of ARF rabbits, activities of gamma-glutamyl transpeptidase and alkaline phosphatase (marker enzymes of brush-border membrane) were decreased. Activities of succinate dehydrogenase, glucose-6-phosphatase, and Na-K ATPase (marker enzymes of mitochondria, endoplasmic reticulum, and basal lateral membrane, respectively) were not affected by CDDP administration. These results suggested that one of the main target sites of CDDP in kidney is brush-border membrane (BBM) along the proximal tubule, that is, not only Na-coupled D-glucose transport carrier protein but also other proteins in BBM.

Acute Kidney Injury↗
PubMed1991

Osmotically regulated taurine content in rat renal inner medulla.

During antidiuresis renal medullary cells were previously found to accumulate large amounts of organic osmolytes, namely sorbitol, myo-inositol, glycerophosphorylcholine (GPC), and betaine. Large quantities of amino acids are also present in the renal medulla, but it has been questionable whether the levels of medullary amino acids are osmotically regulated. Therefore we directly measured 26 different amino acids, as well as sorbitol, myo-inositol, GPC, and betaine alone the corticomedullary axis of rats that were either salt loaded, after infusion of hypertonic NaCl solution, or were hydrated, after infusion of hypotonic NaCl solution. The amounts of sorbitol, myo-inositol, GPC, and betaine are greater in the inner medullas of salt-loaded rats compared with hydrated rats. In addition, the amount of taurine is much greater in the inner medullas of salt-loaded rats. Aspartic acid also increases in salt-loaded rats but to a lesser extent. There are substantial gradients of taurine, aspartic acid, and some of 24 other measured amino acids along the corticomedullary axis. However, taurine and aspartic acid are the only measured amino acids that increase significantly during salt loading.

Amino Acids↗
PubMed1991

[A case of the milk-alkali syndrome with a small amount of milk and magnesium oxide ingestion--the contribution of sustained metabolic alkalosis induced by hypertonic dehydration].

We described a patient with the milk-alkali syndrome induced by the ingestion of small amount of milk (200 ml/day) and ice cream (145 g/day) and the administration of small dose of absorbable alkali (magnesium oxide 2.0 g/day) for the treatment of chronic constipation. The present case shows not only triads, i.e., hypercalcemia (s-Ca 14.3 mg/dl), metabolic alkalosis (s-HCO3- 37.4 mEq/L), and renal insufficiency (s-Cre 2.3 mg/dl) but also hypernatremia (s-Na 161 mEq/L) and hypertonic dehydration after the frequent episodes of elevated body temperature. The milk-alkali syndrome has been defined as the hypercalcemia with a metabolic alkalosis from a high amount of calcium intake and long term administration of absorbable alkali in any form, usually as calcium carbonate for the treatment of peptic ulcer. As the present case could be distinguished from any other cases previously reported with regard to the amount of calcium (0.4 g/day) and alkali (36 mEq/day) intake and the clinical situations that induced the syndrome, we compared the present case with the previous reports, calculating the amount of calcium and alkali intake from milk and absorbable alkali. After the introduction of the H2 blockers for peptic ulceration, the most cases with milk-alkali syndrome had provoked by the smaller amount of calcium than previously reported, which were associated with the treatment of relatively large amount of alkali (50-150 mEq/day), suggesting the role of sustained metabolic alkalosis for the development. In the present case the metabolic alkalosis induced by hypertonic dehydration and enhanced by absorbable alkali intake also could cause an increase of renal tubular reabsorption of calcium and a decrease of ionized calcium which might produce increased secretion of parathyroid hormone followed by vitamin D3 activation and increased Ca absorption from the gut. The metabolic alkalosis might be essential to the development of the milk-alkali syndrome without a high calcium and absorbable alkali intake.

Aged↗